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      microRNA target prediction programs predict many false positives

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          Abstract

          According to the current view, each microRNA regulates hundreds of genes. Computational tools aim at identifying microRNA targets, usually selecting evolutionarily conserved microRNA binding sites. While the false positive rates have been evaluated for some prediction programs, that information is rarely put forward in studies making use of their predictions. Here, we provide evidence that such predictions are often biologically irrelevant. Focusing on miR-223-guided repression, we observed that it is often smaller than inter-individual variability in gene expression among wild-type mice, suggesting that most predicted targets are functionally insensitive to that microRNA. Furthermore, we found that human haplo-insufficient genes tend to bear the most highly conserved microRNA binding sites. It thus appears that biological functionality of microRNA binding sites depends on the dose-sensitivity of their host gene and that, conversely, it is unlikely that every predicted microRNA target is dose-sensitive enough to be functionally regulated by microRNAs. We also observed that some mRNAs can efficiently titrate microRNAs, providing a reason for microRNA binding site conservation for inefficiently repressed targets. Finally, many conserved microRNA binding sites are conserved in a microRNA-independent fashion: Sequence elements may be conserved for other reasons, while being fortuitously complementary to microRNAs. Collectively, our data suggest that the role of microRNAs in normal and pathological conditions has been overestimated due to the frequent overlooking of false positive rates.

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          Most cited references65

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          MicroRNAs: target recognition and regulatory functions.

          MicroRNAs (miRNAs) are endogenous approximately 23 nt RNAs that play important gene-regulatory roles in animals and plants by pairing to the mRNAs of protein-coding genes to direct their posttranscriptional repression. This review outlines the current understanding of miRNA target recognition in animals and discusses the widespread impact of miRNAs on both the expression and evolution of protein-coding genes.
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            A ceRNA hypothesis: the Rosetta Stone of a hidden RNA language?

            Here, we present a unifying hypothesis about how messenger RNAs, transcribed pseudogenes, and long noncoding RNAs "talk" to each other using microRNA response elements (MREs) as letters of a new language. We propose that this "competing endogenous RNA" (ceRNA) activity forms a large-scale regulatory network across the transcriptome, greatly expanding the functional genetic information in the human genome and playing important roles in pathological conditions, such as cancer. Copyright © 2011 Elsevier Inc. All rights reserved.
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              Predicting effective microRNA target sites in mammalian mRNAs

              MicroRNA targets are often recognized through pairing between the miRNA seed region and complementary sites within target mRNAs, but not all of these canonical sites are equally effective, and both computational and in vivo UV-crosslinking approaches suggest that many mRNAs are targeted through non-canonical interactions. Here, we show that recently reported non-canonical sites do not mediate repression despite binding the miRNA, which indicates that the vast majority of functional sites are canonical. Accordingly, we developed an improved quantitative model of canonical targeting, using a compendium of experimental datasets that we pre-processed to minimize confounding biases. This model, which considers site type and another 14 features to predict the most effectively targeted mRNAs, performed significantly better than existing models and was as informative as the best high-throughput in vivo crosslinking approaches. It drives the latest version of TargetScan (v7.0; targetscan.org), thereby providing a valuable resource for placing miRNAs into gene-regulatory networks. DOI: http://dx.doi.org/10.7554/eLife.05005.001
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                Author and article information

                Journal
                Genome Res
                Genome Res
                genome
                genome
                GENOME
                Genome Research
                Cold Spring Harbor Laboratory Press
                1088-9051
                1549-5469
                February 2017
                : 27
                : 2
                : 234-245
                Affiliations
                [1 ]Institut de Génétique Humaine, CNRS UPR 1142, 34396 Montpellier, France;
                [2 ]INSERM, U1183, IRMB, University Hospital St Éloi, 34295 Montpellier, France;
                [3 ]University of Medicine, 34060 Montpellier, France;
                [4 ]Clinical Department for Osteoarticular Diseases, University Hospital Lapeyronie, 34295 Montpellier, France
                Author notes

                Present addresses: 5MSU, The Museum of Natural History, Moscow, Russia, 119991; 6Children's Hospital, Boston, MA 02115, USA

                Corresponding author: herve.seitz@ 123456igh.cnrs.fr
                Author information
                http://orcid.org/0000-0003-3080-1899
                http://orcid.org/0000-0001-8172-5393
                Article
                9509184
                10.1101/gr.205146.116
                5287229
                28148562
                d7dd08d7-e438-41e1-9269-f1463e76f7fd
                © 2017 Pinzón et al.; Published by Cold Spring Harbor Laboratory Press

                This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genome.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

                History
                : 4 February 2016
                : 6 October 2016
                Page count
                Pages: 12
                Funding
                Funded by: Human Frontier Science Program http://dx.doi.org/10.13039/501100000854
                Award ID: CDA-00017/2010-C
                Funded by: CNRS
                Funded by: Sanofi http://dx.doi.org/10.13039/100004339
                Funded by: La Ligue nationale contre le cancer
                Categories
                Research

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